09 [12–68] for CHBV; 47 [11–84] for CHCV,

and 162 [

09 [1.2–6.8] for CHBV; 4.7 [1.1–8.4] for CHCV,

and 16.2 [9.1–24.5] for NAFLD patients respectively) and hepatic steatosis score on biopsy (odds ratio, 95% confidence interval = 30.7 [19.2–42.2] for CHBV; 24.2 [11.5–37.3] for CHCV, and 21.8 [10.1–45.0] for NAFLD patients respectively). Area under the receiver operating characteristics for CAP was 0.683 (0.601–0.757) for steatosis (S) ≥ 6%, 0.793 (0.718–0.856) for S > 33%, and 0.841 (0.771–0.896) for S > 66% respectively for www.selleckchem.com/products/jq1.html CHBV-infected patients. There was no difference in accuracy of CAP for assessing liver fat among CHBV, CHCV, and NAFLD patients. CAP is a novel, non-invasive tool that can detect and quantify steatosis accurately among CHBV, CHCV, and NAFLD patients, the accuracy being similar for all the three groups of patients. “
“TCBOPOP (1,4-bis [2-(3,5-dichaloropyridyloxy)] benzene) an agonist of the constitutive androstane receptor (CAR), produces rapid hepatocyte hyperplasia and hepatomegaly in the absence of hepatic injury. In this study we demonstrate that integrin-linked kinase (ILK), which is involved in transmission of the extracellular matrix (ECM) signaling by way

of integrin receptors, plays an important role in regulating TCPOBOP-induced proliferation of hepatocytes and hepatomegaly. Hepatocyte-specific ILK knockout mice (ILK/liver−/− mice) and wildtype mice (WT) were given a single dose of TCPOBOP (3 mg/kg) by oral gavage. Mice were sacrificed at days 1, 2, 5, and 7 after TCPOBOP administration. WT mice showed maximum proliferation on days 1 and 2, which came back to baseline levels by days 5 and 7 after TCPOBOP administration. The ILK/liver−/− mice, on the other hand, showed a prolonged this website and a sustained proliferative response as evident by an increased number of proliferative cell nuclear antigen assay (PCNA)-positive cells even at days 5 and 7 after TCPOBOP administration. At day 7 the WT mice showed close to a 2.5-fold increase in liver weight, whereas the ILK/liver−/− mice showed a 3.7-fold increase in liver weight. The prolonged proliferative response in the ILK/liver−/− mice seems to be due to sustained induction of CAR leading to sustained induction of c-Myc, which is

known to be a key mediator of TCPOPOP-CAR induced direct liver hyperplasia. Conclusion: The MCE data indicate that ECM-mediated signaling by way of ILK is essential for adjustment of final liver size and proper termination of TCPOBOP-induced proliferation of hepatocytes. (HEPATOLOGY 2011;53:587-595) The liver responds to specific classes of xenobiotics by inducing members of the nuclear hormone receptor superfamily, particularly the pregnane X receptor and the constitutive androstane receptor (CAR).1-3 An ideal candidate for studying xenobiotic metabolism is the halogenated hydrocarbon 1,4-bis [2-(3,5-dichaloropyridyloxy)] benzene (TCPOBOP). TCPOBOP is both a nongenotoxic carcinogen on its own and a potent tumor promoter when combined with genotoxic agents.

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